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T H E

I N D

I A N

A C A

DE M Y O F P E D I

A T

R I C S

Intensive Care Chapter

The IntensivistJ nu y, 2009

Ed toAnil Sachdev

OfficE BEarErsChairperson

Narendra Rungtase et y

Anil Sachdev

T e u eDhiren Gupta

Exe ut ve MembeArun BansalRavi Khanna

Bala RamchandA. K. Jagnany

V. Buche

immed te P t ch pe onPraveen Khilnani

Address or CorrespondenceAnil Sachdev

Dept. o PediatricsCentre or Child HealthSir Ganga Ram Hospital

Rajindra Nagar, New Delhi-60

Email: anilcriticare@hotmail.comWebsite: www.piccindia.org

Message rom Chairman ............................... 01Message rom Secretary ............................... 02

rev ew a t leMyocarditis in Children ................................. 03

P o edu eLaryngeal Mask Airway ................................. 0

Jou n l s nJournal Scan ......................................................

Qu zQuiz on Myocarditis ....................................... . 0

c e repo tPulmonary Arteriovenous Mal ormation 10

Te hnology Upd teNear In rared Spectroscopy .......................... 13

C o n t e n t s

Dear Colleagues,

A happy new year to all o you. I take this opportunity to thank you all orreposing con dence in me and electing me to high o ce o ChairmanIntensive Care Chapter IAP. I eel overwhelmed. I sincerely wish that we cantake this chapter to greater heights, create more opportunity or pediatriciansin critical care and expand the network o training centers or the training. Itmay be relevant to mention that the Ist Asian Congress o Pediatric CriticalCare is being held at Jaipur rom 25 th to 27 th September 2009. The con erence issponsored by World ederation o Pediatric Intensive and Critical Care. I invite

you all to join us in this education east. Visit our website www.picc2009.comto know more about it. I also congratulate my colleagues Dr Anil Sachdevand other members o the executive who have been elected to the Executiveo this chapter. I thank the past chairman or having carried the torch o this chapter to this level .Thanks to Dr Anil or bringing out enthusiasticallyThe Intensivist.

Thanking you and Jai Hind

Narendra RungtaChairmanIntensive care chapter, IAPemail: drnrungta@gmail.com

M ss g f om Ch m n

Intensive Care ChapterIndian Academy of Pediatrics

OfficE BEarErs

N end rungtChairperson

a un B n lExecutive Member

r v Kh nnExecutive Member

B l r m h ndExecutive Member

a. K. J gn nyExecutive Member

V. Bu heExecutive Member

an l s hdevSecretary

P veen Kh ln nImmediate Past

Chairperson

Dh en GuptTreasurer

The Intensivist Newsletter ofIntensive Care Chapter Indian Academy of Pediatrics

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M ss g f om S c y

Dear Colleagues,

I wish you all a very happy and prosperous 2009.It is an honor to get elected to the post o secretary o the IAP IntensiveCare Chapter. I also appreciate the trust bestowed on me to edit the TheIntensivist.For this issue o Intensivist I had to depend on my colleagues and ellows orarticles. It is my sincere request to all the members to contribute articles, casereports or interesting clinical experiences or publication in the Intensivist. Withyour contributions, Intensivist will be an interesting and high quality readingmaterial especially or those working in the periphery providing critical carewith limited resources. It is my wish to trans orm this newsletter to a proper journal and later as an indexed journal. There is an immense need to increase the number o members in the chapter. It

is my experience that lots o youngsters are interested in critical care especiallyin small cities and towns. Current members should stimulate and encouragethem to join the intensive care chapter.Waiting or your support and contributions With regards and thanks

Anil SachdevSecretary and Editor

S u S t a i n i n g t h e l i f e f o r c e

AERO NEB LARYNGEAL MASK EXCELLFEEDY

Nebuliza on Kit Infant Feeding Tube Laryngeal Mask

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Myocarditis in ChildrenDhiren Gupta 1, Garima Garg 2, Col. R. P. S. Tomar 31Consultant Intensivist, 2Fellow Pediatric Critical Care, 3Visiting Fellow Pediatric Critical Care, Pediatric Critical Care Division, Departmento Pediatrics, Centre or Child Health, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi 110 060

ObjectivesReview the basic underlying pathophysiology o myocarditis1.in childrenCharacterize the physiologic derangements, clinical and2.laboratory mani estationsReview the general and speci ic cardiac supportive3.measures and newer modalities available or the treatmento myocarditisSolve the quiz with Per ect 104.

IntroductionMyocarditis is de ned as infammation o the myocardium, whichcan be di use or ocal and is usually due to verity o in ectiousand non-in ectious causes(1). The clinical presentation variesrom asymptomatic ECG abnormalities to haemodynamic

collapse or sudden death. Since most cases are subclinical, thetrue incidence o myocarditis in children is unknown. Criticalcare is an essential component in determining outcomes ore ected children.

EtiologyA large array o in ectious, infammatory and toxic causes o myocarditis has been identi ed ( Table 1). Viral in ections causemost cases o myocarditis. Enteroviruses, most importantlycoxsackie B virus, are the most requent cause o epidemics o viral myocarditis in children.

Pathogenesis The principal mechanism o myocardial damage occurs in threerecognized phases: (a) Initial myocardial injury (b) autoimmunemyocardial injury, during which clinically overt heart ailure maydevelop (c) typical eatures o dilated cardiomyopathy(2).

Direct invasion o the myocardium by cardiotropic viruses viareceptor-mediated endocytosis and are translated intracellularlyto produce viral protein or contribute to myocyte dys unction bycleaving dystrophin ollowing incorporation o the viral genomeinto the cell. Followed by rapid progression to activation o theimmune system, including natural killer cells and macrophages,with subsequent expression o pro-infammatory cytokines suchas interleukin-1, tumour necrosis actorwhich also has a directnegative chronotropic e ect. CD4+ activation results in urthermyocardial cell damage, local infammation and the productiono circulating anti-heart antibodies. Permanent myocardialdamage may be the end result o myocarditis resulting romnecrosis o healthy as well as in ected myocytes leading to dilatedcardiomyopathy.

Clinical ManifestationsMyocarditis is classi ied as ulminant, acute, or chronic(3).Fulminant myocarditis is preceded by a viral prodrome that isollowed by sudden onset o severe hemodynamic compromise.Acute myocarditis has a less distinct onset initially, less severecompromise but is ollowed by a worse outcome than ulminantmyocarditis. Chronic myocarditis can be de ned as persistent(lasting >3 months), recurrent, and latent.

Infectious Immune-mediated Toxic / Hypersensitivity

VirusCoxasackie B Churg-Struss syndrome AntracyclineAdenovirus Infammatory bowel disease CocaineParvovirus Gaint cell myocarditis EthanolHepatitis C Sarcoidosis Heavy metals

HIV SLE InterleukinsBacteria Diabetes mellitus SulphonamidesStreptococcus Thyrotoxicosis Diuretics Treponema pallidum Wegners disease CephalosporinsMycobacterium Sps Takayasu arteritis DobutamineMycoplasma pneumoniaeFungi CandidaCoccidiodesCryptococcusHistoplasmaProtozoal / Parasites Trypanosoma cruzi (Chagas disease)Schistosomiasis

Larva migrans

Review Article

Table 1: Common causes o myocarditis.

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Children may nonspeci c prodromal symptoms o viraemia,including ever, myalgia, coryza or gastroenteritis, associatedwith anorexia, vomiting, and lethargy (Table 2). Older childrenmay have chest pain or abdominal pain. Atypical mani estationssuch as syncope, seizures, and sudden death also have beenreported. Immunization status should be obtained particularlyor diphtheria, poliomyelitis.

Tachycardia in an otherwise healthy child without known originmay be an ominous sign. Other signs o poor tissue per usionare o ten present at presentation in emergency or PICU. O ten

an S3 (ventricular gallop) occurs because o rapid lling o anoncompliant, poorly contracting le t ventricle. Murmurs areless common. Heart sounds may be mu led i concomitantpericarditis is present. Rhythm irregularities may be detected,especially supraventricular tachycardia or ventricular ectopic beats. Tachypnea as a result o pulmonary edema due to le t ventricularailure is a common sign o myocardial ailure in children(4). Otherndings can include wheezing, cough, grunting, nasal faring, andintercostal retraction. Older children may report orthopnea orinability to catch their breath. Cyanosis is rare.

Diagnostic Evaluation

The diagnostic approach or a child with suspected myocarditisincludes strategies to both aid in establishing the diagnosisand rule out disease processes that may mimic myocarditis(a structural cardiac de ect or pericardial e usion). In addition,many o these interventions provide an estimate o myocardialunction and can help in establishing clinical interventions(5,6).Diagnostic ndings are summarized in Table 4.

MonitoringClose and continuous hemodynamic and respiratory monitoringis required or patients su ering with myocarditis. Parameterslike ECG, capillary ll time, urine output, pulse rate and quality,

blood pressure, central venous pressure, and end-tidal CO 2 are essential. Serial lactate level and mixed venous saturationmeasurement should be done when ever available. Invasivepressure monitoring is pre erable in patients with unstablehemodynamics.

Continuous blood pressure monitoring via an arterial catheteris pre erred in children with severe cardiac dys unction,particularly those who require in usions o vasoactive agents.Noninvasive measurements may be inaccurate or impossibleto obtain because o impaired peripheral per usion andvasoconstriction.

Central venous pressure or RA pressure monitoring providesa continual refection o intravascular volume status and is a

good determinant o right ventricular end-diastolic volume or

preload. CVP should be interpreted along with other measures o cardiac unction (heart rate, peripheral per usion, urine output).In critically ill children, the absolute value is not as important asserial measurements and changes in response to interventions.CVP monitoring should be done via the distal lumen o thecatheter. Monitoring can be continual or intermittent, dependingon the availability o intravenous access. Normal CVP values canvary widely in in ants and children, depending on age, disease,

concomitant conditions, and critical care therapies. Any changesin intrathoracic pressure will a ect CVP values; spontaneousrespiration decreases CVP, whereas increased intrathoracicpressure increases CVP. Values lower than expected may ormay not indicate hypovolemia; high CVP values may or maynot indicate hypervolemia. Elevated CVP values may also occurin patients receiving positive pressure ventilation and withthe addition o positive end-expiratory pressure. Conditionsthat increase pulmonary vascular resistance (hypothermia,hypoxemia, acidosis, severe respiratory disease, underlyingpulmonary hypertension) also increase CVP.

Pulmonary arterial pressure monitoring using Swan Ganzcatheter may be considered in highly unstable patients withmultiple vasoactive drugs. Technical di culties and doubt ule ect on outcome minimizes its utility.Repeated echocardiography is a very use ul, noninvasive bedsidetool available to monitor the cardiac status and to adjust fuidtherapy and vasoactive drugs.

Management The rst line o treatment or myocarditis is supportive, symptom-based care(7). General principles o stabilization include inotropicsupport, a terload reduction, anticoagulation and diuresis.

Fluid Management

The goal o fuid management is to maintain an intravascularvolume su cient to preserve preload and ventricular llingwithout overload. In acute or decompensated heart ailure,diuretics are o ten administered because removal o excessintravascular volume may help improve cardiovascular unction.Diuretics are administered cautiously because too rapid aremoval o intravascular fuid can result in hypovolemia andhypotension. Initial dose o urosemide may be at 0.1 to 0.25mg/kg per dose to prevent an excessive reduction in cardiacoutput(7). Doses can be repeated every 6 to 12 hours up to2 mg/kg per dose. Furosemide can also be administered as acontinuous in usion at 0.1 to 0.4 mg/kg/hour, with the additionalbene ts o maintaining a constant serum level and minimizingthe opportunity or sodium retention by the kidneys. Oncethe acute episode o ailure is controlled, other diuretic agentsincluding thiazides and spironolactone, are used.

Inotropic Support

Inotropic agents are administered cautiously because themyocardium is irritable and use o inotropic agents can instigateand/or worsen arrhythmias . (Table 4) When cardiac outputis inadequate, a rapid acting inotropic agent is administered.Dobutamine is o ten used when the primary cause o inadequatetissue per usion is cardiac in origin. Dobutamine improvescontractility and decreases a terload so improving cardiacoutput. A mild increase in heart rate can occur, althoughsigni cant tachycardia is unusual. In children with congestiveheart ailure with patent coronary ar teries, coronary blood fowand oxygen supply to the heart actually increase. Dopamine

Symptoms Signs

Dyspnoea Failure to thriveSweating TachypnoeaPoor eeding TachycardiaRecurrent chest in ections Gallop rhythmOrthopnoea Murmur o mitral regurgitationParoxysmal nocturnal Hepatomegaly

dyspnoea Peripheral oedemaRaised jugular venouspressure

Table 2: Symptoms and signs o cardiac ailure in childhood.

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has both inotropic and vasopressor properties and is use ul inpatients who are in shock with cardiac dys unction and associatedmild to moderate hypotension. Dopamine is not routinely usedto treat poor cardiac contractility i blood pressure is normal;in this instance, a purely inotropic agent is recommended.Milrinone, a phosphodiesterase inhibitor, improves myocardialdiastolic unction, resulting in improved ventricular relaxationand lling times. There is improvement in cardiac index andreduction in systemic vascular resistance in both pediatric andneonatal populations with the use o milrinone. It is also less

arrhythmogenic than many other agents, making it inotrope o choice in many centers. Severe shock may require the additiono epinephrine, although it increases myocardial oxygenconsumption and workload and chances o arrhythmias.

Levosimendan is a promising new agent in a new class o medications known as calcium sensitizers(8). Traditional inotropicagents that increase intracellular calcium are associated withincreased oxygen consumption, impaired myocardial relaxation,and dysrhythmias. Levosimendan is novel in that it increases bothinotropy and vasodilation without increasing calcium levels ormyocardial oxygen demand. The enhancement o contractilityoccurs by binding to troponin C and increasing myo lamentsensitivity to calcium. Levosimendan causes vasodilatation viaopening o potassium-dependent ATP channels. Levosimendan

has been used sa ely and e ectively in adults, with recent studiesdemonstrating improved mortality. Isolated case reports havebeen published o its use in children with severe heart ailurepostoperatively and in the setting o a dilated cardiomyopathy.

Arrhythmia ManagementRhythm disturbances can be li e threatening and must be treatedaggressively. Ventricular ectopy, ventricular tachycardia, andheart block can develop in children with myocarditis(9). Rhythmdisturbance can result rom myocardial infammation, hypoxia,inotropic therapy, electrolyte disturbance or a combination o those actors. Regardless o the cause, tachyarrhythmias mustbe controlled. For patients with supraventricular tachycardia,adenosine or electro-version is recommended depending onhemodynamic status. In children with recurring supraventriculartachycardia, amiodarone is considered. Ventricular ectopyis o ten treated with amiodaron or lidocain i ormer is notavailable. Digoxin should be used with great caution in acutephase myocarditis since it can induce or worsen ventriculararrhythmias. I digoxin is used, the loading dose should be nomore than 75% o the normal total loading dose. I completeatrioventricular block or second-degree block with inadequate

per usion develops, a temporary pacemaker may be used.

Table 3: Investigations or suspected myocarditis.Test CommentsECG Sinus tachycardia, low voltage QRS, ST-T, QT changes,conduction de ects, chamber hypertrophyChest X-ray Cardiomegaly (Subacute, chronic), Pulmonary edemaEchocardiogram Chamber dilatation, poor contractility, thrombusCardiac MRI scan Myocardial infammation and myocyte injuryCK-MB, Troponin CK low sensitivity and speci city, Trop-I high speci cityFull blood count Leucocytosis, lymphocytosis

Viral antibody titers Serial rising titers IgM antibodiesViral PCR Detect viral genome in tracheal aspirate. High sensitivityEndomyocardial Invasive, lack standardization, immuno-histochemistry biopsy use ul

Table 4: Commonly used drugs in myocarditis in PICU.Drugs DosesVasopressors/ Inotropes *Dopamine 5 10 g /kg /minDobutamine 5 10 g /kg /minEpinephrine 0.05 2 g /kg /minVasodilators*Nitroprusside 0.5 10 g /kg /minNitroglycerine 1 10 g /kg /minMilrinone ** 50 g /kg / min over 10 min

Followed 0.25 0.75 g /kg /minEnalapril 0.1 mg / kg daily PO BiD. Increase over

2 wks to max 0.5/ kg / dose BiDCaptopril In ants: 0.1 0.5 mg/ kg/dose q 812hMax 4mg/kg/dayChild: 0.1 2 mg/kg/day q 8-12 h (6.25-25 mg/day)

DiureticsFrusemide 0.1 1 mg / kg /hr***.

0.5 2 mg/ kg/ dose q 6 hrIVIG 1- 2 g/ kgDigoxin****

In ant or child: 25 40 g /kgAdolescent: 0.5 1mg in divided doses.Maintainance dose: 5 -10 g /kg/day q 12 h

*In usion pump use recommended, **Inodilator, ***Continuous in usion IVIG intravenous immunoglobulin, ****IV dose 75% o mentioned dose, digitalization dose initially ollowed by q 12 h

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Oxygenation, Ventilation, and AirwayManagementOxygen delivery should be maximized. The method o deliverydepends on the childs age, severity o illness and hemodynamicstatus. Oxygen should be provided with nasal cannula, acemask or over-head hood. Most children will require some ormo positive pressure ventilation by non invasive or invasivemethods. Continuous in usion o Sedation like midazolam andanalgesia like morphine o ten with muscle relaxant are requiredor mechanical ventilation.

Effects of Positive-pressure Ventilation in Left-ventricular Failure

Positive pressure ventilation with PEEP is o ten bene cial inpatients with systemic ventricular dys unction due to diminishedLV a terload and optimal lung recruitment. Tidal volumes shouldbe maintained in the range o 6-8 mL/kg to avoid overdistension,which could increase PVR and RV a terload. Furthermore,evidence suggests that shorter inspiratory times may augmentLV illing in patients with systemic ventricular dys unction.Because alterations in thoracic pressure may have opposing

hemodynamic e ects, all ventilatory maneuvers should becare ully evaluated with respect to systemic oxygen deliveryand hemodynamic e ects.

Effects of Positive-pressure Ventilation in Right-ventricular Failure

Alterations in ventricular compliance make patients with RVailure particularly sensitive to changes in venous return causedby adjustments in intrathoracic pressure. Ventilation strategiesused or patients with RV ailure should aim to minimize meanairway pressure while maintaining lung volume at unctionalresidual capacity, where lung unction, PVR and RV a terloadare optimal. Spontaneous inspiration enhances diastolic fowand thus overall cardiac output in these patients; there ore, early

extubation can be bene cial. Alternative modes o ventilationsuch as negative-pressure or high- requency jet ventilation havebeen studied. As high- requency jet ventilation reduces meanairway pressure and PVR while maintaining a similar PaCO 2, itmay be ideally suited to patients with RV dys unction and/orpulmonary hypertension.

Antibody therapy/ Immuno-supp-ressiveTherapyAs discussed in pathogenesis, immune dys unction plays amajor role in the evolution o myocarditis. So there is scopeor immunosuppressive therapies to shorten the course andlessen the severity o illness(10). IVIG suppresses the immuneresponse, replace antibodies, enhance viral clearance, neutralizepathogens, and enhance clearance o infammatory cytokinesthat contribute to myocyte destruction. Improvement in le tventricular unction and 1-year survival rate in patients withbiopsy-proven myocarditis has been demonstrated a tertreatment with a single, high dose o intravenous immuneglobulin (1-2 g/kg body weight). Immunoglobulins are sa erand better tolerated than corticosteroids or other immuno-suppressive agents. Although the bene ts o IVIG in pediatricmyocarditis remain unproven, IVIG continues to be an importantadjunct therapy in children with acute viral myocarditis. Otherimmunosuppressive agents like cyclsporin and azathioprinehave been also tried.

AnticoagulationReports o the use o anticoagulants in patients with myocarditisare largely anecdotal. Severely compromised ventricular unctionand stasis o blood fow, as can occur in depressed myocardialunction, can increase the risk or thrombus ormation.

Mechanical Support Devices andTransplantationMechanical assist devices and ECMO may be needed in ewpatients when medical treatment ails. Orthotropic cardiactransplant in needed or end-stage disease in dilated cardiomy-opathy patients.

Prognosis and progression The survival rate in children and adults with myocarditis isapproximately 80%(11). Survival a ter 72 hours in patientsnot requiring ECMO is as high as 97%.Some centers havehad a 1-year survival rate o 80% in children who requiredmechanical circulatory support. Un ortunately, survival todischarge does not imply ull recovery. Survival in children withdilated cardiomyopathy ranges rom 60% to 70% at 1 year to34% to 56% at 5 years. Viral persistence in the myocardiumhas been associated with progressive impairment o le tventricular unction and is predictive o adverse outcomes.Immunosuppression has not been shown to be e ective asroutine treatment or acute lymphocytic myocarditis. Early trialso antiviral therapies, such as inter eron, suggest a potentialtherapeutic role but require urther investigation.

References

Aretz HT, Billingham ME, Edwards WD, et al: Myocarditis: a1.histopathologic de nition and classi cation. Am J CardiovascPathol 1987;1:3-14Batra AS, Lewis AB. Acute myocarditis. Curr Opin Pediatr2.2001; 13:234-239Leonard EG. Viral myocarditis. Pediatr In ect Dis J 2004; 23:665-3.666Feldman AM, McNamara D. Medical progress: myocarditis. N4.Engl J Med 2000; 343:1388-1398Park MK, Troxler RG. Pediatric cardiology or practitioners. 4th5.ed. St Louis, MO: Mosby; 2002:289-290Drucker NA, Newburger JW. Viral myocarditis: diagnosis and6.management. Adv Pediatr 1997; 44:141-169 Tobias JD, Deshpande JK, Johns JA, Nichols DG. Infammatory7.heart disease. In: Nichols DG, Ungerleider RM, Spevak PJ, etal, 2nd ed. Critical Heart Disease in In ants and Children.Philadelphia, PA: Mosby; 2006:899-925Schwartz SM, Wessel DM. Medical cardiovascular support8.in acute viral myocarditis in children. Pediatr Crit Care Med2006;7:S12-S16Bohn D, Macrae D, Chang AC. Acute viral myocarditis: mechanical9.circulatory support. Pediatr Crit Care Med 2006;7: S21-S24Udi N, Yehuda S. Intravenous immunoglobulin - indications10.and mechanisms in cardiovascular diseases. AutoimmunRev 2008; 7:445-52Bruns LA, Christant MK, Lamour JM, et al : Carvedilol as therapy11.in pediatric heart ailure:an initial multicenter experience. J

Pediatr 2001;138:505-511

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International Critical Care Congress &15th Annual Conference of Indian Society

of Critical Care Medicine

Pre- Conference Workshop: February 18th to 19th, 2009Conference: 20th to 22nd February, 2009

Laryngeal Mask AirwaySunil Dutt, Abdul Azeem KhanFellows, Pediatric Critical Care Divison, Department o Pediatrics, Centre or Child Health, Sir Ganga Ram Hospital, Rajinder Nagar,New Delhi

Laryngeal mask airway (LMA) is a device used by anesthetistsand pediatricians or ventilating children during resuscitationand during surgical procedures is a reusable device, madeprimarily o medical grade silicone rubber and is entirely latexree. Disposable devices are also currently available.

The LMA consists o three main components: an airway tube,mask and mask infation line. The airway tube is large-bore tubewith a 15 mm standard male adaptor. Its other end is tted witha specially shaped cu , which is infated and defated via a valveon the end o the infation line. The mask is designed to con orm

to the contours o the hypopharynx with its lumen acing thelaryngeal opening. The LMA is designed to be a minimallystimulating and invasive device.

The LMA has been ound to provide a clear upper airwayprovided that:

Prior to insertion, it is correctly defated to orm a smoothfat wedge shape that passes easily around the back o thetongue and behind the epiglottis.Protective re lexes are su iciently depressed to permitsmooth insertion. The user has acquired the necessary skill to insert the LMA.

IndicationsElective surgical procedures where ace masks are currentlyused or tracheal intubation is not necessary.Known or unexpected di cult airway situation.When tracheal intubation is precluded by lack o availableexpertise or equipment or when attempts at trachealintubation have ailed.During bronchoscopy in children who have tubes too smallto allow sa e passage o bronchoscope through them.

ContraindicationsIt should not be used in the resuscitation or emergency

situation in patients who are pro oundly unconscious(i.e. require rapid sequence intubation).Patients who resist LMA insertion.

PrecautionsCare ul handling should be done as it is made o silicone,which can be easily torn or per orated. There ore contactwith sharp or pointed objects should be avoided. The LMA valve should not be exposed to any cleaningsolutions, as these substances are absorbed by the LMAmaterial resulting in premature valve ailure.

RisksRisk o aspiration is always there, as LMA does not protectthe airway rom the e ects o regurgitation. There ore cricoidpressure must always be maintained during the use and gastricdecompression must be done prior to insertion o the LMA.

LMA insertionWatch the accompanying CD.

LMA size selection guidelinesSize Patient weight

1 Up to 5 kg1 5 to 10 kg

2 10 to 20 kg2 20 to 30 kg

3 30 to 50 kg

Intubating LMA This is a relatively new addition or the di cult airway. It permits

placement o a tracheal tube a ter appropriate positioning o theLMA. All interventions that are per ormed through a tracheal tubecan be then undertaken, including administration o medications,ventilation etc. This is currently available or adult use only.

Procedure

visit us: www.criticare2009.orgvenue: Jay Pee Palace Convention Center

CritiCare-2009

ISCCM

riticareAGRA 2009

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Journal ScanVikas BansalFellow Pediatric Critical Care, Pediatric Critical Care Division, Department o Pediatrics, Centre or Child Health, Sir Ganga Ram Hospital,Rajinder Nagar, New Delhi 110 060

Saline instillation before tracheal suctioningdecreases the incidence of ventilator-associatedpneumonia.Pedro Caruso, Silvia Denari, Soraia A. L. Ruiz, Sergio E. Demarzo,Daniel Deheinzelin. Crit Care Med 2009; 37:3238

This study compared the incidence o ventilator-associatedpneumonia (VAP) with or without isotonic saline instillationbe ore tracheal suctioning. Incidence o endotracheal tubeocclusion and atelectasis was also compared as secondaryobjective. It was a randomized clinical trial conducted in a medicalsurgical intensive care unit o an oncologic hospital. Patientsrequiring mechanical ventilation >72 hours were included anddivided into two groups: a saline group that received instillationo 8 mL o saline be ore tracheal suctioning and a control groupwhich did not. VAP was diagnosed based on clinical suspicionand con rmed by bronchoalveolar lavage quantitative culture. The incidence o atelectasis on daily chest radiography andendotracheal tube occlusions were recorded. One hundredthirty patients were assigned to the saline group and 132 to thecontrol group. The baseline demographic variables were similarbetween groups. The rate o clinically suspected VAP was similarin both groups. The incidence o microbiological proven VAP wassigni cantly lower in the saline group (23.5%vs10.8%; p= 0.008)(incidence density/1000 days o ventilation 21.22 vs 9.62; p